There is ample evidence that a relationship exists between duct hyperplasia and carcinoma of the pancreas, and Sommers has indicated that an experimental model for the production of pancreatic duct hyperplasia would point the way to a better understanding of the mechanisms involved. This application presents a new model which permits such a study. Chronic duct obstruction (CDO), without the development of chronic pancreatitis, has been produced in the pancreas of the Syrian Golden hamster (SGH) by wrapping the head of the gland with cellophane tape. Ligation of the duct is not involved. Preliminary studies have revealed that CDO alone can induce ductal hyperplasia and metaplasia, as well as ductular proliferation and the initiation of nesidioblastosis. Specific aims of the research proposed in this application are: (1) to study the changes in the ducts, ductules, islets and acinar cells of the pancreas at varying intervals during the course of chronic duct obstruction. (2) to examine the inter-relationship of chronic obstruction and the carcinogen N-nitrosobis(2-oxypropyl) amine (BOP) during the time course of tumor development. These studies will involve a combined morphological, morphometric, biochemcial, and immunocytochemical approach. The objective of this proposal is to specify the role played by duct obstruction and hyperplasia in relation to carcinogenesis, and to use our model as a means of studyng pancreatic cell populations in order to identify the precursor cell of pancreatic neoplasms. Significance. We believe that this new model and its modification by carcinogenic substances will produce results which will have great significance in our understanding of precursor lesions and etiologic factors in pancreatic cancer. This is of particular importance in the early recognition of this disease in man.